Vasospasm in traumatic brain injury.

Given the large societal burden from morbidity and mortality associated with traumatic brain injury (TBI), this disease entity has been the focus of extensive research over the past decades. Since primary injury in TBI is preventable whereas secondary injury is treatable, most of the research effort has been targeted at identifying factors that contribute to secondary injury and ways to minimize their deleterious effects. Whether post-traumatic vasospasm is one such factor is open for debate. Although radiological or anatomical vasospasm following head injury has been repeatedly demonstrated using various diagnostic techniques, its clinical significance is still under investigation. At the present time, no proven treatment regimen aimed specifically at decreasing the potential detrimental effects of post-traumatic vasospasm exists. Although calcium channel blockers have shown some promise in decreasing death or severe disability in those with traumatic subarachnoid haemorrhage, whether their mechanism is by minimizing vasospasm is open to speculation. Therefore, currently, vigilant diagnostic surveillance, including serial head CT's and the prevention of secondary brain damage due to hypotension, hypoxia, and intracranial hypertension, may be more cost effective than attempting to minimize post-traumatic vasospasm.

Inhibition of c-Jun N-terminal kinase pathway attenuates cerebral vasospasm after experimental subarachnoid hemorrhage through the suppression of apoptosis.

BACKGROUND: Recent studies have demonstrated that apoptosis in cerebral arteries could play an essential role in cerebral vasospasm after subarachnoid hemorrhage (SAH) and that SP600125, an inhibitor of c-Jun N-terminal kinase (JNK) could suppress apoptosis. The present study examined whether SP600125 could reduce cerebral vasospasm through the suppression of apoptosis. METHOD: Fifteen dogs were assigned to 3 groups: control, SAH, and SAH + SP600125 (30 micromol/l). SAH was induced by the injection of autologous blood into the cisterna magna on day 0 and day 2. Angiograms were evaluated on day 0 and day 7. The activation of the JNK pathway and caspase-3 were also evaluated using Western blot. To determine the distribution, TUNEL staining and immunohistochemistry for phosphorylated c-jun and cleaved caspase-3 were performed. FINDINGS: Severe vasospasm was observed in the basilar artery of the SAH dogs. SP600125 reduced angiographic and morphological vasospasm and reduced the expression of cleaved caspase-3, thereby suppressing apoptosis. CONCLUSIONS: These results demonstrate that SP600125 attenuates cerebral vasospasm through the suppression of apoptosis, which may provide a novel therapeutic target for cerebral vasospasm.

Neuroprotective effect of hyperbaric oxygen in a rat model of subarachnoid hemorrhage.

Acute brain ischemia after subarachnoid hemorrhage (SAH) induces oxidative stress in brain tissues. Up-regulated NADPH oxidase (NOX), a major enzymatic source of superoxide anion in the brain, may contribute to early brain injury after SAH. We evaluated the effects of hyperbaric oxygen (HBO) on protein expression of gp91(phox) catalytic subunit of NOX, lipid peroxidation as a marker of oxidative stress, and on neurological and neuropathological outcomes after SAH. Twenty-nine male Sprague-Dawley rats (300 to 350 g) were randomly allocated to control (sham operation), SAH (endovascular perforation), and SAH treated with HBO groups (2.8 ATA for 2 hours, at 1 hour after SAH). Cerebral blood flow was measured using laser Doppler flowmetry. Rats were sacrificed after 24 hours and brain tissues collected for histology (Nissl staining and gp91 (phox) immunohistochemistry) and biochemistry. Mortality and neurological scores were evaluated. Neuronal injury associated with enhanced gp91 (phox) immunostaining was observed in the cerebral cortex after SAH. The lipid peroxidation product, malondialdehyde, accumulated in the ipsilateral cerebral cortex. HBO treatment reduced expression of NOX, diminished lipid peroxidation, and reduced neuronal damage. HBO caused a drop in mortality and ameliorated functional deficits. HBO-induced neuroprotection after SAH may involve down-regulation of NOX and a subsequent reduction in oxidative stress.

Moderate head injury: an overview.

This review summarizes currently available epidemiologic, clinical, pathologic, and outcome data in patients with moderate head injury (MHI, GCS 9-12). This important subset comprises about 20% of head injuries in the United States. Affected patients usually are young, and most injuries are due to vehicular accidents. Current evidence (mortality rate and outcome) from various studies suggests an apparent dichotomy within the MHI category (9-10 vs 11-12). The former is more in keeping with the favorable subgroup of severe head injuries, and the latter is more appropriate to the mild head injury group. Should there be a reclassification based on this dichotomy? This is obviously important for clinical management and prognostication in these patients. The experimental evidence for a pathologic and biochemical substrate of MHI is reviewed. It is becoming increasing evident that biochemical mediators of secondary neuronal injury in MHI are at least as important as those attributed to severe head injury, but MHI may be more amenable to therapy. It may be prudent, therefore, to direct further effort to this subgroup of patients. Although additional study is required, the pattern of recovery in MHI as determined by extant neurobehavioral studies is analyzed.

Arterial saccular aneurysm model in the rabbit.

Saccular aneurysms arising from the common carotid artery in the neck at the origin of the internal carotid artery were created in male rabbits using the stump of a ligated external carotid artery. These stumps were intraluminally perfused with varying concentrations of porcine pancreatic elastase for 45 minutes via a microcatheter introduced into the femoral artery. The aneurysms were allowed to mature for 2 to 12 weeks. Gross examination and histologic studies confirmed the presence of an aneurysm in all 15 experiments. Ninety-two percent (12 of 13) of the aneurysms studied by postoperative angiography were shown to be angiographically patent: 40% of all aneurysms were noted to be patent at harvest; and the remainder showed evidence of intraluminal thrombus. On histologic examination, all aneurysms showed complete loss of elastic lamina without evidence of fibrosis or scarring.

Cocaine-induced aneurysmal rupture: an emergent negative factor in the natural history of intracranial aneurysms?

Recent statistics from the National Institute on Drug Abuse indicate that cocaine abuse continues to be a significant public health problem. Between 1988 and 1990 at Grady Memorial Hospital in metropolitan Atlanta, Georgia, we identified 12 patients in whom subarachnoid hemorrhage was temporally related to cocaine abuse. All 12 patients had underlying cerebral aneurysms that had ruptured. Currently, the incidence of ruptured intracranial aneurysms in patients with cocaine-induced subarachnoid hemorrhage is 84.9% (mean age, 31.1 years; overall mortality, 60.5%). Hypertension is the likely precursive factor in cocaine-induced aneurysmal rupture. Cocaine abuse appears to be a significant negative factor in the natural history of cerebral aneurysms, especially in young adults. We review the epidemiology of cocaine-induced subarachnoid hemorrhage and its effects on the cerebral circulation, and suggest guidelines for patient management.

Bifrontal osteoplastic craniotomy utilizing the anterior wall of the frontal sinus: technical note.

There are various flaps for bifrontal exposure of the anterior fossa classically described in the neurosurgical literature. This article describes a bifrontal split osteoplastic flap that is characterized by removal of the anterior wall of the frontal sinus without the placement of burr holes on the external surface of the frontal bone. The procedure is safe and rapid, gives the same exposure as other techniques, and allows a superior cosmetic result.

Barrier disruption in the major cerebral arteries during the acute stage after experimental subarachnoid hemorrhage.

The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the basilar arteries were studied during the acute stage after SAH. SAH was induced in rats by injecting fresh autologous blood into the cisterna magna. Horseradish peroxidase (HRP) was given intravenously before killing the animals to assess the integrity of the barrier. In the basilar arteries taken from the animals that were killed 30 minutes after the cisternal injection of either mock cerebrospinal fluid or arterial blood, HRP reaction products were diffusely observed in the subendothelial spaces and smooth muscle layers. At 5 hours after the blood injection, no permeation of HRP into the subendothelial space was observed. Endothelial cell transcytosis seemed to be the important mechanism for HRP permeation into the subendothelial space rather than the opening of interendothelial junctions. The disruption of the blood-arterial wall barrier in the major cerebral arteries after SAH may be involved in the pathogenesis of vasospasm.

Ectopic pituitary gland simulating a suprasellar tumor.

A case report of ectopic pituitary gland in the suprasellar region of a normal 39-year-old woman with persistent headaches is presented. The embryological development of the pituitary gland is briefly reviewed, with a discussion of the relevant literature. No previous report of normal pituitary tissue in a suprasellar location in the absence of tumor could be found.

Intradural perimedullary arteriovenous fistulas (type IV spinal cord arteriovenous malformations).

Intradural perimedullary arteriovenous fistulas (Type IV spinal cord arteriovenous malformations (AVM's)) are rarely reported in the literature and occasionally are classified together with Type II AVM's as intradural spinal cord AVM's. The authors report eight cases of Type IV spinal cord AVM's managed over a 2-year period. Seven of these AVM's were surgically obliterated, with intraoperative angiography being used as an adjunct; one other patient was managed using endovascular therapy. One of these lesions was definitely and another possibly the result of trauma; a malformation in a newborn infant was clearly congenital. The authors believe that the pathophysiological mechanisms and anatomical features of these lesions represent a unique spinal vascular anomaly that must be recognized angiographically to plan appropriate therapy.

A rapid and modifiable technique for regional exposure in cerebral surgery. Technical note.

The authors describe a technique by which a properly demarcated regional cerebral exposure may be performed rapidly and safely. The method involves a linear scalp incision of varying length and orientation and a circumferential craniotomy of variable size and shape centered about a single burr hole. While providing for rapid exposure with reduced blood loss, the vascular integrity of the wound is also better preserved, allowing for rapid healing of the scalp. This technique provides satisfactory unilateral exposures of most cerebral sites not located in the vicinity of the frontal sinus or the sphenoid wing.

Terson's syndrome: a reversible cause of blindness following subarachnoid hemorrhage.

Terson's syndrome refers to the occurrence of vitreous hemorrhage with subarachnoid hemorrhage (SAH), usually due to a ruptured cerebral aneurysm. Although it is a well-described entity in the ophthalmological literature, it has been only rarely commented upon in the neurosurgical discussion of SAH. Fundus findings are reported in a prospective study of 22 consecutive patients with a computerized tomography- or lumbar puncture-proven diagnosis of SAH. Six of these patients had intraocular hemorrhage on initial examination. In four patients vitreous hemorrhage was evident on presentation (six of eight eyes). In the subsequent 12 days, vitreous hemorrhage developed in the additional two patients (three of four eyes) due to breakthrough bleeding from the original subhyaloid hemorrhages. The initial amount of intraocular hemorrhage did not correlate with the severity of SAH. Two of the six patients with intraocular hemorrhage died, whereas five of the 16 remaining SAH patients without intraocular hemorrhage died. Of the four survivors with intraocular hemorrhage, three showed gradual but significant improvement in their visual acuity by 6 months. The fourth underwent vitrectomy at 8 months after presentation and had a good visual result. With modern and aggressive medical and microsurgical management, Terson's syndrome should be recognized as an important reversible cause of blindness in patients surviving SAH.

Intracranial aneurysms in sickle-cell anemia: clinical features and pathogenesis.

Intracranial aneurysms are an unusual complication of sickle-cell anemia; only 15 patients have been described in the world literature. An additional 15 patients with sickle-cell anemia and subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms are presented. There was a high incidence of multiple aneurysms (60%); some of which were in unusual locations. The clinical and pathological features of this series of patients have provided a paradigm for acquired aneurysm formation that may be applicable to other intracranial aneurysms. Thirteen patients underwent craniotomy and clip ligation; the perioperative management of these patients is discussed. Of these 13, eight had a good recovery, three were left with moderate disability, one patient died of surgical complications, and one died of complications related to sickle-cell anemia. Two of the 15 patients died of SAH. The authors propose that endothelial injury from the abnormal adherence of sickle erythrocytes to the endothelium is the initiating event in arterial wall injury. Subsequently, there is fragmentation of the internal elastic lamina and degeneration of the smooth-muscle layer. Hemodynamic stress at these loci of arterial wall damage results in aneurysm formation. This hypothesis also explains other cerebrovascular manifestations of sickle-cell anemia, namely vaso-occlusive disease and hemorrhage without aneurysm formation. Pathological material from this series and data from the literature are presented to support this hypothesis.

Frontal sinus approach to the orbit. Technical note.

The authors have previously advocated a supraorbital approach to tumors of the orbit. In this paper, they describe a technique in which they take advantage of a large frontal sinus as a means of entering the orbit without the necessity of intracranial exposure, as required by the more conventional supraorbital approach. This is achieved without frontal burr holes, allowing for a superior cosmetic result. The anterior wall of the frontal sinus is removed, and with it the roof of the orbit as a single bone flap. A case in which this technique was used is described.

Intravenous fluid loading as prophylaxis for paradoxical air embolism.

Paradoxical cerebral air embolism has been described in neurosurgical operations performed on patients in the seated position. This problem is thought to result most often from a probe-patent foramen ovale. It has been postulated that right atrial pressure exceeds left atrial pressure when paradoxical air embolism occurs. A study is described in which intravenous fluid loading is compared with routine fluid management in 20 patients undergoing neurosurgical operations in the seated position. In order to investigate if intravenous fluid loading would decrease the risk of paradoxical air embolism during neurosurgical operations on seated patients, 20 patients were assigned randomly to two groups: 10 patients received normal intravenous fluid replacement (1220 +/- 102 ml), and 10 received augmented fluid replacement (2800 +/- 400 ml). Right atrial and pulmonary capillary pressures were monitored for evidence of an interatrial pressure gradient that would force air emboli from the right atrium into the left atrium via a probe-patent foramen ovale. Four of 10 patients receiving routine fluid administration developed right atrial pressure greater than pulmonary capillary wedge pressure (and hence, indirectly, greater than left atrial pressure), whereas none of the 10 patients with augmented fluid loading developed this condition (p = 0.04). The authors conclude that augmented intravenous fluid loading may be effective in preventing systemic air embolism during neurosurgical operations performed on patients in the seated position.

Head injury mortality in two centers with different emergency medical services and intensive care.

The authors report data collected prospectively on 551 cases of head injury in New Delhi, India, and 822 cases in Charlottesville, Virginia. The mortality rate, adjusted for initial severity of injury, was 11.0% in New Delhi versus 7.2% in Charlottesville (p less than 0.02). There was a striking similarity in mortality rates at both centers when comparing patients with the least severe head injuries and those with the most severe injuries according to the motor score of the Glasgow Coma Scale (GCS M). However, in the group with an abnormal but purposeful motor response (GCS M = 5), the mortality rate was 12.5% in New Delhi versus 4.8% in Charlottesville (p less than 0.01). The relative absence of prehospital emergency care and the delay in admission after head injury in New Delhi are cited as two possible causes for the differences in mortality rates in this subgroup of patients with "moderate" head injuries.

Pericapillary arteriovenous malformations angiographically manifested as cerebral venous malformations.

Cerebral venous malformations have been diagnosed by angiographic features and are considered to be a benign anomaly. However, ample evidence indicates that stroke or similar symptomatology occurs in patients harboring a cerebral vascular malformation that was diagnosed angiographically as a venous malformation. The purpose of the study is to confirm the presence of a pericapillary arteriovenous malformation in these patients by analyzing the clinical history and surgical findings and correlating them with histological features. Thirteen patients were included in this study. Each patient fulfilled four criteria: 1. the patient was neurologically symptomatic; 2. the angiographic diagnosis was a venous malformation; 3. at operation, shunting arterioles (50-100 microns) were found to contribute to the malformation; and 4. histologically, a mixture of venous channels and arterioles with arterioles directly connected to venules was found. Based on the above findings, the malformation present in the 13 patients can be termed a 'pericapillary arteriovenous malformation'. Its angiographic distinction from the cerebral venous malformation requires technological advancement in the capability of magnifying images of arterioles and venules, along with improvement in image resolution.

Extracranial repair of cerebrospinal fluid rhinorrhea.

There has been a recent renewal of interest in the extracranial repair of cerebrospinal fluid rhinorrhea because of the relatively high morbidity associated with the transcranial approach. The authors describe an extracranial approach that involves packing of the sphenoid and ethmoid sinuses on the side of the CSF leak. A case of successful treatment of CSF rhinorrhea by this method is presented. The extracranial approach may be advantageous for the repair of CSF rhinorrhea and the authors advocate an increase in its utilization by neurosurgeons and otolaryngologists working as a team.

Cranial migration of a lumboperitoneal shunt catheter.

We describe a patient with pseudotumor cerebri for which a lumboperitoneal (LP) shunt was placed. After a pseudomeningocele was noted at the lumbar incision site, an LP shunt revision was done, at which time migration of the catheter into the thecal sac was noted. Three months later, radiologic studies revealed cranial migration of the LP shunt into the posterior fossa. We believe no similar complication has been reported.